SHOCKING UPDATE! Statin drugs that lower cholesterol levels interfere with brain function and can induce symptoms interpreted as MS, ALS and Parkinson's Disease. It is also being shown that cholesterol levels have nothing to do with heart disease!! Dr Duane Graveline

Recently, the parmamafia have encouraged use of statins for MS, for the anti inflammatory effect.

It is madness to prescribe a drug FOR MS, that causes brain damage, and neurological symptoms!!

08/06/09

There was a time when I believed that prescribed steroid treatments were beneficial, and I attributed remission of symptoms to this drug. In clearer moments, I recalled that I had recovered from several serious episodes, before and after diagnosis, much faster, with NO drug therapy! After finding considerable evidence in research that steroids have no positive effect on course of ms, and many negative side effects, I ceased all drug therapy (1974). 
We humans tend to link observations to support our needs, and forget that just because two things happen at the same time, does not mean they are necesarily related .... 
Conflict of interest: Readers need to be aware of the influence of financial support, sponsorship, advertising ... most articles state possible conflict of interest. Is science served by authors who design studies to support a position that has already been decided? 

Hans Selye warns that experimental medicine is based upon the principle that, if a change occurs only in those subjects receiving a certain treatment, then the treatment must he regarded as the cause of the change. Here, the important fallacy is that what you gave is not necessarily what acted. Errors in experimental design or procedure, play some part in almost every fallacy, Selye also warns of dangerous traps in scientific reasoning, and how easy it is to miss the discovery of what is clearly before us. 

Articles I find interesting ...  

Rasmnsky M and Sears TA, Internodal Conduction in Undissected Demyelinated Nerve Fibres. J Physiol(Lond) 227:323-350, 1972 - intracellular sodium accumulation offered as the explanation for (affected activity) seen in demyelinated fibres - position of nodes inferred from assumption that nodes are the only sites of inward membrane current - 3% of normal myelin sufficient for normal function .. 
em... steroids affect the balance of sodium and potasium (mineralocorticoids) vital for potential difference needed for signal transmission ... 

Anat Achiron, Elon Pras, R Gilad, Ilan Ziv, Mathilda Mandel, Carlos R Gordon, Shlomo Noy, Ida Sarova-Pinhas & Eldad Melamed, Open Controlled Therapeutic Trial of Intravenous Immune Globulin in Relapsing-Remitting Multiple Sclerosis. Arch Neurol 49:1233-1236, 1992. During 12 month study period immune globulin treated patients with MS improved by an average of 0.3 Kurtzke units, while untreated control patients worsened by 0.2 units. Improvement in the immune globulin treated group, as well as the aggravation in the control group, as compared with their scores before the treatment was not statistically significant ... p 1235. 

Nishihori T, Abdo-Matkiwsky M , Fleishman SB, Blum RH, Severe action tremor related to interferon-alpha 2b therapy for malignant melanoma. .Am J Clin Oncol. 2005 Oct;28(5):526. 
Interferon (IFN)-alpha 2b is used for adjuvant therapy in malignant melanoma. Neurotoxicity as a side effect has been well described. Resting and action tremor related to interferon have been reported but are relatively uncommon. We report a case of a delayed-onset interferon-related action tremor in a patient with malignant melanoma. 

Arne-Bes MC, [Neurotoxic effects of medications: an update] [Article in French] Rev Med Liege. 2004;59 Suppl 1:118-23. 
Unite des Maladies Musculaires et Electrophysiologie, Service de Neurologie, Hopital Rangueil, Toulouse. arne-bes.mc@chu-toulouse.fr Peripheral neuropathy is a common neurotoxic effect of medications. Antineoplastic agents and antiretroviral medications are most often involved: platinum compounds, vinca alkaloids, taxols and nucleoside reverse transcriptase inhibitors. These agents cause a dose-related axonal polyneuropathy. Symptoms are indicative of a predominantly sensory or sensory-motor neuropathy which in some cases is accompanied by dysfunction of autonomic nervous system. Depending on dosage and agent used symptoms resolve completely or not. Neurotoxic effect can appear immediately during or shortly after administration of the drug but sometimes after cessation of chemotherapy. In all cases the neuropathy alters the quality of life. A general predisposition for developing a neuropathy has been observed in nerves previously damaged by diabetes mellitus, alcohol or in inherited neuropathy. Within the past five years, some cases of neuropathy caused by alpha-interferon, statins or tacrolimus have been reported. Although rare, these aetiologies should be considered by physicians and the drugs removed when others causes of neuropathy have been excluded. Few cases of peripheral neuropathy have been recently reported with metronidazole, dapsone, nitrofurantoin or colchicin. Thalidomide induces a dose-dependant sensori-motor length-dependent axonal neuropathy(stiffness in legs-em). It should be judiciously used with close neurologic monitoring. Little is known about the mechanisms responsible for the development of neuropathy. Up to now, no drug is available to prevent or cure drug-induced neuropathies.  

Wichers MC, Koek GH, Robaeys G, Verkerk R, Scharpe S, Maes M, IDO and interferon-alpha-induced depressive symptoms: a shift in hypothesis from tryptophan depletion to neurotoxicity. Mol Psychiatry. 2005 Jun;10(6):538-44.  Department of Psychiatry and Neuropsychology, Maastricht University, Maastricht, The Netherlands.  m.wichers@sp.unimaas.nl 
Studies show that administration of interferon (IFN)-alpha causes a significant increase in depressive symptoms. The enzyme indoleamine 2,3-dioxygenase (IDO), which converts tryptophan (TRP) into kynurenine (KYN) and which is stimulated by proinflammatory cytokines, may be implicated in the development of IFN-alpha-induced depressive symptoms, first by decreasing the TRP availability to the brain and second by the induction of the KYN pathway resulting in the production of neurotoxic metabolites.  

Penny Whiting, Roger Harbord, Caroline Main, Jonathan J Deeks, Graziella Filippini, Mathias Egger and Jonathan AC Sterne, 
Accuracy of magnetic resonance imaging for the diagnosis of multiple sclerosis: systemic review, British Medical Journal, 2006; 332: 875-8. f 
... not all patients who experience a first attack will develop the disease and currently no treatment has been shown to delay conversion to clinically definite multiple sclerosis or impact on long term disability. 

Valentine AD, Meyers CA, Neurobehavioral effects of interferon therapy. Curr Psychiatry Rep, 2005 Oct;7(5):391-5. 
... most common causes of treatment discontinuation of Interferon (IFN) therapy ... associated with neuropsychiatric side effects including cognitive dysfunction and mood syndromes of varying severity ... approach 50% in recent studies. Effective management of IFN-induced neuropsychiatric side effects should involve pretreatment screening and interval assessment during therapy. 

The "re - discovery" of myelin repair in the year 2000, links repair of myelin to chemical treatment. 
The process of repair of myelin has been proven spontaneous. When we accept this fact, we can apply it to recovery. That’s my story. 

June 2000   The Boston Globe reports work claiming to be the first evidence of remyelination ... 
Laurence M Howard, Amy J Miga, Carol L Vanderluget, Mauro C Dal Canto, Jon D Laman, Randolph J Noelle & Stephen D Miller (1999).  J Clin Invest 103:281-290.  Mechanisms of immunotherapeutic intervention by anti-CD40L (CD154) antibody in an animal model of multiple sclerosis. Supported by US Public Health Service/National Institutes of Health Research grant NS34819 (to S.D.Miller), NS30871 (to S.D.Miller), AI37075 (to R.J.Noelle), and NS13011 (to M.C.Dal Canto), and by National Multiple Sclerosis Society grants RG2275 (to S.D.Miller), RG2893 (to M.C.Dal Canto), and 5-38229 (to R.J.Noelle). 
REVIEW - by EM 
Experimental subjects are mice immunized with relapsing experimental autoimmune encephalitis  (R-EAE) [man made virus] to cause demyelination.  Controls were hamsters  ... 
Clinical signs of disease were evaluated for up to 40 days ... by observation 
Team members determined peak of acute disease or remission ... by observation  ...  mice were sacrificed 25 days after  immunization with anti-CD40L (CD154) antibody ... extensive areas of demyelination and remyelination were observed. Authors conclude that the repair of myelin was the result of the injections ...  

June 2000   Los Angeles Times reports that scientists repair MS-type damage for the first time. 
Researchers report that treating the mice with the antibodies for five weeks caused myelin to re-grow.  
Over that brief period, new myelin repaired about 25 per cent of damaged areas.  
Arthur E Warrington, Kunihiko Asakura, Allan J Bieber, Bogoljub Ciric, Virginia Van Keulen, Srini V Kaveri, Robert A Kyle, Larry R Pease & Moses Rodriguez, Proc Natl Acad Sci 7(12):6820-6825. (2000). Human monoclonal antibodies reactive to oligodendrocytes promote remyelination in a model of multiple sclerosis. Supported by National Institutes of Health Grant NS24180 and Acorda Therapeutics. 
REVIEW - by EM 
Mice 4-6 weeks old were injected with Theiler's murine encephalomyelitis vaccine (TMEV) resulting in plaque forming damage. 
5 - 8 months later, animals were given a single injection of human monoclonal antibodies (mAbs). 
5 weeks after injection the animals were sacrificed. 
Area of remyelination in spinal cord sections was estimated to be 47.7% in 10-12 spinal cord sections per mouse, and 40.0% in all 32 sections. Estimated that new myelin repaired about 25 per cent of damaged areas. 
Authors conclude that treating the mice with the antibodies caused myelin to re-grow ... 

Review research on myelin repair: JOURNAL REFERENCES 
1 - Spontaneous repair of damaged myelin begins in 17-19 days. 
    [This means that myelin repair was underway long before injections began.] 

2 - Movement speeds repair. 
    [Unrestrained animals heal naturally.] 

3 - Clinical condition is not related to disease activity. 
    [Human observation can not determine the peak of disease activity, 
    nor, when disease activity ceases.] 

Past research projects were designed to study damage to myelin as it is observed in multiple sclerosis, by using human tissue in vitro, or post mortem tissue samples. These studies using experimental animals, and normal controls, fixed tissue samples for study at regular intervals, with the electron microscope. Spontaneous repair of myelin was observed in mice (small mammals) in 1 week, and in cats and rabbits (large mammals) in 7-31 days. Humans are classed as large mammals.  Many authors have observed that thin repair is sufficient for resumption of normal function in experimental animals, and, in humans. 

One study (Bunge et al, 1961) observed that the neurological condition of the experimental animal begins to improve at a time when remyelination begins, and has returned to normal by the time most axons are at least thinly repaired. 

Paul Freedman writes that society honours the re-discoverer more than the unexpected discoverer, not only after the discovery has finally been accepted, but more or less permanently. eg: Rosslyn Franklin & DNA, PBS feature, Candace Pert & peptides, read Molecules of Emotion)  
 
In the New Millennium, we are ignoring the discovery that is clearly behind us. Myelin repairs itself! Repair is spontaneous & movement can speed healing & recovery.